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SWHR Emerging Scholars in Women’s Health Research Award  Symposium

May 6 @ 9:15 am - May 9 @ 11:00 am EDT

Part of the OSSD Annual Meeting

This event is taking place on Monday, May 6 at 3:15-5:00 p.m. CET, in-person in Bergen, Norway.

The Society for Women’s Health Research (SWHR) is dedicated to advancing women’s health through science, policy, and education while promoting research on sex differences to optimize women’s health. The SWHR Emerging Scholars in Women’s Health Research Award is given to trainees whose abstracts submitted to the OSSD Annual Meeting demonstrate research excellence in addressing important knowledge gaps in health and disease areas that disproportionately, differently, or exclusively affect women. This inaugural year for the award centers on Aging & Women’s Health.

Presentations will include:

Adolescent Hormonal Contraceptive Administration Impacts Prefrontal Cortex Maturation and Risk-assessment in Female Rats.

  • Speaker: Rachel Gilfarb, MS, Department of Psychology, The Ohio State University

Pregnancy-associated Oxidative Stress and Inflammation are not Associated with Impaired Maternal Neuronal Activity or Memory Function

  • Speaker: Jessica L. Bradshaw, PhD, Department of Pharmaceutical Sciences, University of North Texas Health Science Center

Genes that Escape X Chromosome Inactivation are Associated with Alzheimer’s Disease Endophenotypes: Findings from ROSMAP

  • Speaker: Mabel Seto, PhD, Department of Neurology, Massachusetts General Hospital

 

REGISTER

The OSSD 2024 Annual Meeting is taking place in Bergen, Norway this May. Find more information about the OSSD 2024 Annual Meeting here.

This event is part of OSSD Conference, that requires registration and fee to attend.

The SWHR Emerging Scholars in Women’s Health Research Award  Symposium is one of two events SWHR is hosting during the meeting. Check out the other event, on May 5: “SWHR Pre-Conference Symposium: Lights, Camera, and Action to Improve Women’s Heart Health.”

Details

Start:
May 6 @ 9:15 am EDT
End:
May 9 @ 11:00 am EDT
Event Categories:
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Website:
https://www.ossdweb.org/annual-meeting

2024 SWHR Emerging Scholars Awardees

Jessica L. Bradshaw, PhD 
SWHR Emerging Scholars in Women’s Health Research Awardee
Jessica L. Bradshaw, PhD 
SWHR Emerging Scholars in Women’s Health Research Awardee

Dr. Jessica Bradshaw is a Postdoctoral Research Associate completing her postdoctoral training in neuroendocrinology, behavior, and rodent models of intermittent hypoxia under the primary mentorship of Dr. Rebecca Cunningham at the University of North Texas Health Science Center in Fort Worth, Texas. Dr. Bradshaw was classically trained as an immunologist during her graduate studies and combines this expertise and experience with her research interests in maternal cardiovascular and brain health during pregnancy and post-pregnancy. Her postdoctoral studies were supported by an American Heart Association postdoctoral fellowship examining the role of innate immune activation in preeclampsia, a hypertensive disorder of pregnancy. Dr. Bradshaw’s current studies are focused on the intersection of hypoxia and inflammatory processes in maternal brain health during pregnancy and the postpartum period. Her research has contributed to our understanding of the impact of gestational immune activation on maternal cardiovascular outcomes and fetal growth dynamics, as well as maternal brain plasticity and behavior during pregnancy and post-pregnancy. Dr. Bradshaw is a tireless advocate for women’s health research and maternal health equity and enjoys spending time with her four children, two dogs, and supportive spouse.

 

Abstract: Pregnancy-associated Oxidative Stress and Inflammation are not Associated with Impaired Maternal Neuronal Activity or Memory Function 

Jessica L. Bradshaw [1], E. Nicole Wilson [1], Jennifer J. Gardner [1], Steve Mabry [1], Selina M. Tucker [1], Nataliya Rybalchenko [1], Edward Vera Jr. [1], Styliani Goulopoulou [2], Rebecca L. Cunningham [1].  

[1] UNT Health Science Center, Fort Worth, Texas, USA  

[2] Loma Linda University, Loma Linda, California, USA 

Pregnancy is associated with neural and behavioral plasticity, systemic inflammation, and oxidative stress. The impact of inflammation and oxidative stress on maternal neural and behavioral plasticity are unclear. We hypothesized that the maternal hippocampal CA1, a brain region associated with cognition, would be protected from pregnancy-associated inflammation and oxidative stress, mediating stable peripartum cognitive performance. Cognition was tested using novel object recognition, Morris water maze, and open field behavior tasks in nulliparous (nonpregnant), pregnant (near term), and primiparous (two-months post-pregnancy) Sprague-Dawley rats. Plasma and CA1 proinflammatory cytokines were measured via MILLIPLEX magnetic bead assay. Plasma oxidative stress was measured via advanced oxidation protein products assay. CA1 markers of oxidative stress, neuronal activity, and apoptosis were quantified via western blotting. Our results demonstrate CA1 oxidative stress was elevated in pregnant compared to nulliparous rats but was equivalent levels in pregnant and primiparous rats. Reproductive state did not impact CA1 inflammatory cytokines, neuronal activity, apoptosis, or memory function. Spatial learning was impaired while anxiety-like behavior was reduced in primiparous rats. Our data highlight long-term effects of pregnancy on maternal cognitive performance and suggest maternal hippocampal CA1 is protected from systemic inflammation but vulnerable to peripartum oxidative stress. Funding: NIH R01 HL146562, T32 AG020494; AHA 903250, 9

Rachel Gilfarb, MS 
SWHR Emerging Scholars in Women’s Health Research Awardee
Rachel Gilfarb, MS 
SWHR Emerging Scholars in Women’s Health Research Awardee

Rachel Gilfarb received her Bachelor of Arts degree from Vanderbilt University in 2018, where she majored in Neuroscience and minored in Women’s and Gender Studies. Currently, she is a PhD candidate at The Ohio State University in the lab of Dr. Benedetta Leuner. Her thesis work examines how adolescent hormonal contraceptive administration in female rats affects the development of the prefrontal cortex. Following her thesis defense in July 2024, she plans to pursue a career in science communication.

 

Abstract: Adolescent Hormonal Contraceptive Administration Impacts Prefrontal Cortex Maturation and Risk-assessment in Female Rats 

Rachel Gilfarb [1], Sanjana Ranade [1], Abby Biddle [1], Marrisa Smail [1], Meredith Stewart [1], Abhishek Rajesh1, Elizabeth Dybas [1], Courtney Dye [1], Kathryn M. Lenz [1], Benedetta Leuner [1].  

[1] The Ohio State University  

Millions of individuals take hormonal contraceptives (HCs) often starting at adolescence when ovarian hormones have important effects on prefrontal cortex (PFC) maturation. Yet, there is a fundamental lack of information about the consequences of hormonal alterations with adolescent HC use on PFC development. To address this gap, we examined molecular and functional markers of cortical maturation in female rats treated with HCs in adolescence. Intact female Sprague-Dawley rats were randomly assigned to receive daily subcutaneous injections of either vehicle or HCs (10 µg ethinyl estradiol + 20 µg levonorgestrel) for the duration of adolescence from postnatal day (PND) 35-56. Blood and brain tissue was collected at PND 57 and behavioral assays completed between PND 57-63. HC treatment was effective, as vaginal lavage indicated disrupted estrous cycling and ELISA quantification showed suppression of serum luteinizing hormone in HC-treated rats. Further, in HC treated rats, liquid chromatography/mass spectrometry detected low serum estradiol levels and HC presence in serum and the brain. Within the medial PFC, gene expression profiling with NanoString nCounter custom panel revealed differentially expressed genes with HC treatment, including genes related to glial function, synaptic plasticity, and immune signaling. mPFC immunolabeling for myelin (MBP) and oligodendrocytes (CC1) was found to be increased in HC-treated rats, while Iba1 (microglia) immunolabeling and cell complexity was reduced. HC treatment diminished risk-assessment behavior in the elevated plus maze and novelty-induced hypophagia paradigm. Overall, we show that use of a widely used pharmaceutical (HCs) during a vulnerable developmental period (adolescence) influences PFC maturation, which may contribute to altered risk-assessment behavior. These data have the potential to enhance user agency by pointing to consequences of adolescent HC use not previously identified. Funding: R21 HD109618 

Mabel Seto, PhD 
SWHR Emerging Scholars in Women’s Health Research Awardee
Mabel Seto, PhD 
SWHR Emerging Scholars in Women’s Health Research Awardee

Dr. Mabel Seto is a postdoctoral fellow in the Department of Neurology at Brigham and Women’s Hospital. She received her Ph.D. in Pharmacology from Vanderbilt University, where she utilized multi-omic analyses to identify genetic and molecular modifiers of Alzheimer’s disease risk. Since her Ph.D., she has largely focused on using computational approaches to perform AD research with the goal of identifying new targets for AD drug discovery. She is currently in the lab of Dr. Rachel Buckley, and her present work and interests are related to sex differences in AD, particularly how genes expressed on the X chromosome affects AD endophenotypes. She was also recently awarded an Alzheimer’s Association Research Fellowship to study how parental history of dementia influences offspring AD risk.

Genes that Escape X Chromosome Inactivation are Associated with Alzheimer’s Disease Endophenotypes: Findings from ROSMAP 

Mabel Seto [1],[2], Michelle J. Clifton [2], Gillian T. Coughlan [1], Ting-Chen Wang [2], Reisa A. Sperling [1], Yanling Wang [4], David A. Bennett, Timothy J. Hohman [2], Hyun-Sik Yang [1], Logan Dumitrescu [2], Rachel F. Buckley [1]  

[1] MGH 

[2] Vanderbilt University 

[4] Rush University  

 Alzheimer’s disease (AD) disproportionately affects women. Women possess two X chromosomes, with one randomly silenced across each cell for dosage compensation. X chromosome inactivation (XCI) is not complete, and XCI-escaping genes provide a promising avenue of discovery for biological pathways driving sex-specific AD risk. Using bulk RNAseq from dorsolateral prefrontal cortex tissue, Aβ plaque and tau tangle pathology, and antemortem longitudinal cognition data in a matched sample from ROSMAP (N=648, age-at-deathmean(SD)=87.5(6.5)), we assessed the association between 216 reported XCI-escaping genes and Aβ and tau at autopsy, and longitudinal cognition in linear regression and mixed-effects models. Analyses were sex-stratified and FDR-corrected. 22 genes were associated with Aβ (20 female-specific, 2 male-specific), 49 genes with tau (43 female, 6 male), and 48 genes with cognitive decline (46 female, 2 male). In women, 40% (8/20) were protective against Aβ, 56% (24/43) against tauopathy, and 43% (20/46) against cognitive decline. Of note, higher GRIPAP1 expression was associated with lower Aβ (β=-0.18, p=0.02) and tau (β=-0.21, p=0.001), and slower cognitive decline (β=0.02, p=0.04) in women whereas ATP11C expression was associated with higher Aβ (β=0.19, p=0.03) and tau (β=0.15, p=0.03), and faster cognitive decline (β =-0.02, p=0.03). Altogether, this study presents evidence that studying the X chromosome is integral to understanding female resilience and vulnerability to AD pathology. This study was supported by the NIH New Innovator Award (DP2AG082342).